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. Author manuscript; available in PMC: 2020 Feb 1.
Published in final edited form as: Hypertension. 2019 Feb;73(2):390–398. doi: 10.1161/HYPERTENSIONAHA.118.12084

Figure 6. GATA4 is required for GRP78-mediated promotion of hypertrophic growth.

Figure 6.

A. GATA4 protein expression was increased in the GRP78 transgenic hearts in response to pressure overload. Control and TG mice of 8–10 weeks old were subjected to TAC and western blotting was performed a week later. N = 4. B. GATA4 protein level was upregulated by GRP78 overexpression in NRVMs. GRP78 was overexpressed by adenovirus-mediated infection. The cells were then treated by PE for 24 hours. N = 9. C. GRP78 knockdown led to decrease in GATA4 protein expression. N = 5. D. Knockdown of GATA4 in NRVMs diminished GRP78-mediated hypertrophic response. GRP78 was overexpressed by adenoviral infection and GATA4 was silenced by siRNA transfection. PE treatment was conducted for 24 hours. Immunostaining was done to detect α-actinin. N = 50–80. E. Knockdown of GATA4 reduced GRP78-induced Anf upregulation. F. GRP78 expression enhanced GATA4-dependent Anf promoter activity. An Anf promoter-driven luciferase plasmid was transfected to HEK-293T cells, along with pcDNA3.1 expressing GATA4. Co-transfection of GRP78 led to more profound elevation of luciferase activity, indicating GRP78 potentiates GATA4-dependent Anf induction. N = 3–4. *, p < 0.05; ***, p < 0.001.